Empyema thoracis is an accumulation of frank pus in the pleural space. Occurrence of complications such as bronchopleural fistula (BPF) following necrotizing pneumonia is not uncommon in pediatric patients. Failure to diagnose latent BPF is common. High level of suspicion and preventive measures to avoid likely complications is the key to success. This case report underscores the need to diagnose a latent BPF and also highlights the importance of one lung ventilation in an infant in suspected cases of BPF.

Keywords: Bronchopleural, fistula, latent, ventilation

How to cite this article:Patil SS, Kulkarni SB, Dhamangaonkar AC. The importance of diagnosis of latent bronchopleural fistula in a child with empyema thoracis for thoracotomy. Med J DY Patil Univ 2017;10:187-90

Empyema thoracis is an accumulation of frank pus in the pleural space [1] which is a serious problem in the pediatric population in developing countries.[2],[3] The etiology is pneumonia, tuberculosis, pneumothorax, trauma, and iatrogenic. Treatment options for empyema include tube thoracostomy, thoracotomy, or video-assisted thoracoscopic surgery.[4],[5],[6],[7] A bronchopleural fistula (BPF) is a communication between the pleural space and the bronchial tree.[6] Although rare, BPFs are both diagnostically and therapeutically challenging.[8],[9] The most common cause of BPF is the postoperative complication of pulmonary resection, followed by lung necrosis after infection, persistent spontaneous pneumothorax, and tuberculosis. Its diagnosis may require some special investigations. The existence of a BPF increases the risk of contamination of the contralateral lung thus necessitating its isolation during surgery.[7] One lung ventilation (OLV) in an infant confronts the anesthetist with further set of challenges.

Case Report

In this case report, a 10-month-old female child, third by birth order was brought by the mother with chief complaints of fever and cough with expectoration for 1 month, not responding to medication. This child was diagnosed to have loculated empyema and was posted for thoracotomy. She had a history of repeated episodes of cough since day 17 of birth. There was no history of breathlessness, hemoptysis, tuberculosis, or tuberculosis contact. She was poorly built and nourished. On examination, her pulse rate was 132/min regular, good volume; the respiratory rate was 48/min abdominothoracic with no rib retraction. A dull note was elicited on percussion in the right 3rd, 4th, 5th intercostal spaces. Bronchial breath sounds were auscultated over the right infrascapular and infraaxillary region. The liver was palpable 2 cm below the sixth intercostal space. The investigations showed a hemoglobin concentration of 12.3 g/dl, a total leukocyte count of 36,800/mm 3 with a differential count of 45% polymorphs, and 55% lymphocytes and platelet count of 482,000/mm 3. The tuberculin hypersensitivity test was negative. The arterial blood gas analysis showed pH (7.512)/PaCO2 (24.5 mmHg)/PaO2 (117 mmHg) HCO3 (19.2 mmol/L)/SaO2 (99%)/BE (−1.9). The saturation on air was 97%. The chest radiograph (CXR) showed consolidation and fluid bronchogram in the right costophrenic angle [Figure 1]. The high-resolution computed tomography scan (HRCT) of the chest revealed 4.7 cm × 3.1 cm × 4.3 cm loculated empyema in superior segment of the right lower lobe [Figure 2].

A decision was made to use a single–lumen tube and ventilate both the lungs. The patient was premedicated with injection glycopyrrolate (4 µg/kg), injection midazolam (30 µg/kg), and injection fentanyl (3 µg/kg). The patient was induced with injection propofol (3 mg/kg) and given injection vecuronium (0.01 mg/kg) after confirming adequate ventilation. The trachea was intubated with a regular 4 mm uncuffed endotracheal tube (ETT). The anesthesia was maintained on oxygen, nitrous oxide, and sevoflurane with vecuronium. Fifteen minutes after the commencement of surgery in the lateral position, there was sudden desaturation (SaO2 60%) and a rise in the end-tidal CO2 (68 mmHg). The surgeon was asked to stop the surgery. The child was ventilated with 100% oxygen. Endotracheal suctioning revealed copious blood tinged aspirate. This ventilation and suctioning were repeated 2–3 times. Thereafter, there was some improvement in saturation (SaO2 70%). Direct laryngoscopy was performed and the position of the ETT was reconfirmed. Even after the above, the saturation was persistently low (SaO2 77%) and the end-tidal CO2 was high (54 mmHg). The thoracotomy was closed and an intercostal drain was inserted. The reason behind the desaturation was not evident at that instance. Hence, an immediate postoperative chest radiograph was requested [Figure 3]. It revealed opacification and collapse of the unaffected lung.

This event was probably due to contamination of the unaffected normal lung. The arterial blood gas sample revealed respiratory acidosis pH (7.23)/PaCO2 (58 mmHg)/PaO2 (96 mmHg)/HCO3 (16 mmol/L)/SaO2 (78%)/BE (−12). The existence of a latent BPF was suspected. The other causes suspected were rupture of a subpleural bleb causing pneumothorax or iatrogenic injury during surgery. The patient was hemodynamically stable throughout. A decision to electively ventilate the patient to facilitate expansion of the normal lung was taken. She was shifted to the intensive care unit on a ventilator on pressure synchronized intermittent mandatory ventilation mode. The peak inspiratory pressures were kept between 15 and 20 cm of H2O, so as to generate a tidal volume of 7 ml/kg, respiratory rate of 25/min with I: E of 1:2.5, and positive end-expiratory pressure (PEEP) of 4 cm of H2O. Endotracheal suctioning and nebulization were continued. The patient was weaned off and extubated the same evening. A chest radiograph 12 h postoperatively showed bilaterally well-expanded lungs [Figure 4]. Thereafter, the child had an uneventful recovery in the ward. The intercostal drain was removed on day 3 and was discharged on day 14 of surgery.

The clinical presentation of BPF is divided into acute, subacute, and delayed or chronic forms.[8] When acute, BPF can be a life-threatening condition due to asphyxiation from pulmonary flooding or tension pneumothorax. It is characterized by the sudden appearance of dyspnea, cough with expectoration, hypotension and subcutaneous emphysema. There is also shifting of the trachea and mediastinum and persistence of air leak.

Diagnosis of BPF is challenging. There are various diagnostic modalities for the same. Details mentioned in [Table 1].[9],[10]

The first principle of therapeutic management of a BPF is to address any immediate, life-threatening conditions, such as endobronchial contamination, pulmonary flooding, and tension pneumothorax. This is done by placing the patient with the affected side dependent and performing adequate pleural drainage, antibiotics, nutritional supplementation, and adequate ventilatory management. The principles of mechanical ventilation in a case of a BPF are to maintain adequate ventilation and oxygenation while reducing the fistula flow for facilitating its repair, to attain lowest effective tidal volume, lowest level of PEEP, minimum mechanical breaths per minute and maximum spontaneous breaths per minute, shortest inspiratory time, to allow intermittent mandatory ventilation (avoid control ventilation) and permissive hypercapnia.[8]

OLV in infants can be performed by various techniques which include the use of single–lumen ETT, balloon-tipped bronchial blockers such as Fogarty embolectomy catheter and arndt endobronchial blocker, double-lumen endobronchial tubes (marraro tubes for age below 3 years), and univent tubes.[11]

Infants have soft, easily compressible lungs. Their residual volume is closer to functional residual capacity. In infants, ventilating the healthy lung in dependent position can lead to decrease in lung compliance and increase in airway closure even during tidal breathing. Their small size results in the decrease in hydrostatic pressure gradient between dependent and nondependent lung. Therefore, there is a loss of the favorable response of increasing perfusion to the dependent ventilated side while reducing the perfusion in the pathologic lung, leaving infants susceptible to hypoxia during OLV while placed in lateral decubitus position. Hence, access for ventilating and providing oxygen on the pathologic side must be maintained during OLV.[11]

In our case, the existence of a BPF remained undiagnosed on chest radiograph and CT scan. Thoracoscopy and thoracotomy are not absolute indications for OLV and considering the increased risk of hypoxemia due to V/Q (ventilation –perfusion) mismatch in infants, we decided to ventilate both the lungs. The events that occurred intraoperatively suggested that there was either a BPF which was missed on CT or an occult fistula (opened on IPPV) or iatrogenic injury during surgery. Other cause though unlikely, was rupture of subpleural bleb secondary to infection causing spontaneous pneumothorax as the patient was hemodynamically stable. Thereafter, there was contamination with the debris from the affected lung causing collapse of the normal lung. Repeated suctioning and favorable postoperative ventilation may have helped the closure of the fistula and reexpansion of the collapsed lung.

Thus, if there is any suspicion of BPF on HRCT or CXR, one should call for additional investigations such as bronchoscopy. With the advent of multidetector computed tomography or virtual bronchoscopy which is noninvasive, it is possible to confirm the above diagnosis. OLV should be provided in all cases of BPF. Vigilance and agility are warranted to deal with complications if they occur.